Question

MD19 [Jul98] [Mar99] [Feb00] [Jul01] [Jul04] NSAIDs:

A. Exhibit no selectivity for COX 1 & 2
B. Exert renal effects other than effect on afferent arterioles
C. Cause renal toxicity separate to inhibition of prostaglandins
D. Aspirin & ketorolac irreversibly bind COX1 & 2
E. Directly cause gastrointestinal ulceration

Answer 1

NSAIDs work by inhibiting the enzymes involved in pain and inflammation, blocking the synthesis of prostaglandins. They can have side effects such as gastrointestinal ulcers, bleeding, and kidney damage. Aspirin irreversibly binds to the enzymes, and NSAIDs can cause both renal effects and gastrointestinal ulceration.

Step-by-step explanation:

NSAIDs, or nonsteroidal anti-inflammatory drugs, work by inhibiting the enzymes cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2), which are involved in pain and inflammation. Aspirin, ibuprofen, and naproxen are examples of NSAIDs. They block the synthesis of prostaglandins, which are responsible for inflammation and pain. However, long-term use of NSAIDs can have side effects such as gastrointestinal ulcers, bleeding, and kidney damage.

Specifically addressing the options in the question:

1. NSAIDs exhibit no selectivity for COX-1 and COX-2, meaning they inhibit both enzymes.
2. NSAIDs can have renal effects other than their effects on afferent arterioles, such as kidney damage.
3. NSAIDs can cause renal toxicity to separate from their inhibition of prostaglandins.
4. Aspirin irreversibly binds to both COX-1 and COX-2, meaning its effects are long-lasting.
5. NSAIDs can directly cause gastrointestinal ulceration.

Answer 2

The answer of the given statement that " MD19 [Jul98] [Mar99] [Feb00] [Jul01] [Jul04] NSAIDs" is C. Cause renal toxicity separate to inhibition of prostaglandins

Explanation:

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) can have various effects on the renal system. Option C is correct because NSAIDs, in addition to inhibiting prostaglandins, can cause renal toxicity independent of their effect on prostaglandins.

The inhibition of prostaglandins, specifically prostaglandin synthesis, is a mechanism through which NSAIDs can contribute to renal issues.

Let's briefly review the other options:

A. This statement is incorrect. NSAIDs do exhibit selectivity for COX-1 and COX-2. COX-1 is involved in the protection of the gastric mucosa and renal function, while COX-2 is associated with inflammation.

B. This statement is incorrect. NSAIDs, by affecting prostaglandin levels, can exert effects on the afferent arterioles in the kidneys, influencing renal blood flow.

D. This statement is incorrect. While aspirin irreversibly binds COX-1, ketorolac is a reversible COX inhibitor.

E. This statement is correct to some extent. NSAIDs, including aspirin, can contribute to gastrointestinal ulceration as a side effect, but it's not a direct cause. The inhibition of prostaglandins, which play a role in maintaining the integrity of the stomach lining, contributes to this side effect.

Therefore, option C is the most accurate representation of NSAIDs' renal effects.